Maffeis C
Department of Paediatrics, University of Verona, Polyclinic B Roma, Italy.
Eur J Pediatr. 2000 Sep;159 Suppl 1:S35-44. doi: 10.1007/pl00014361.
The epidemic diffusion of obesity in industrialised countries has promoted research on the aetiopathogenesis of this disorder. The purpose of this review is to focus mainly on the contribution that European research has made to this field. Available evidence suggests that obesity results from multiple interactions between genes and environment. Parents obesity is the most important risk factor for childhood obesity. Twin, adoption, and family studies indicated that inheritance is able to account for 25% to 40% of inter-individual difference in adiposity. Single gene defects leading to obesity have been discovered in animals and, in some cases, confirmed in humans as congenital leptin deficiency or congenital leptin receptor deficiency. However, in most cases, genes involved in weight gain do not directly cause obesity but they increase the susceptibility to fat gain in subjects exposed to a specific environment. Both genetic and environmental factors promote a positive energy balance which cause obesity. The relative inefficiency of self-adapting energy intake to energy requirements is responsible for fat gain in predisposed individuals. The role of the environment in the development of obesity is suggested by the rapid increase of the prevalence of obesity accompanying the rapid changes in the lifestyle of the population in the second half of this century. Early experiences with food, feeding practices and family food choices affect children's nutritional habits. In particular, the parents are responsible for food availability and accessibility in the home and they affect food preferences of their children. Diet composition, in particular fat intake, influences the development of obesity. The high energy density and palatability of fatty foods as well as their less satiating properties promotes food consumption. TV viewing, an inactivity and food intake promoter, was identified as a relevant risk factor for obesity in children. Sedentarity, i.e. a low physical activity level, is accompanied by a low fat oxidation rate in muscle and a low fat oxidation rate is a risk factor of fat gain or fat re-gain after weight loss.
Further research is needed to identify new risk factors of childhood obesity, both in the genetic and environmental areas, which may help to develop more effective strategies for the prevention and treatment of obesity.
肥胖症在工业化国家的流行促使人们对这种疾病的病因发病机制展开研究。本综述的目的主要是聚焦欧洲研究在该领域所做的贡献。现有证据表明,肥胖是基因与环境之间多种相互作用的结果。父母肥胖是儿童肥胖最重要的风险因素。双胞胎、收养及家族研究表明,遗传因素能够解释个体间肥胖差异的25%至40%。在动物身上发现了导致肥胖的单基因缺陷,在某些情况下,在人类中也得到证实,如先天性瘦素缺乏或先天性瘦素受体缺乏。然而,在大多数情况下,与体重增加相关的基因并不会直接导致肥胖,而是会增加暴露于特定环境中的个体脂肪增加的易感性。遗传和环境因素都会促进正能量平衡,从而导致肥胖。能量摄入自我适应能量需求的相对低效是易患个体脂肪增加的原因。本世纪下半叶,随着人群生活方式的迅速改变,肥胖患病率迅速上升,这表明环境在肥胖发展中起作用。早期的食物体验、喂养方式和家庭食物选择会影响儿童的营养习惯。特别是,父母负责家中食物的供应和获取,他们会影响孩子的食物偏好。饮食组成,尤其是脂肪摄入量,会影响肥胖的发展。高脂肪食物的高能量密度和适口性以及它们较低的饱腹感会促进食物消费。看电视是一种促进不活动和食物摄入的行为,被确定为儿童肥胖的一个相关风险因素。久坐不动,即身体活动水平低,会伴随着肌肉中脂肪氧化率低,而低脂肪氧化率是体重减轻后脂肪增加或重新增加的一个风险因素。
需要进一步研究以确定儿童肥胖在遗传和环境方面的新风险因素,这可能有助于制定更有效的肥胖预防和治疗策略。